ICL 7.1: Eye & Retina Flashcards

1
Q

what are the parts of the eye?

A

out side
1. cornea

  1. anterior chamber
  2. iris
  3. pupil
  4. lens
  5. retina
    inner most
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2
Q

what is inside the anterior chamber of the eye?

A

aqueous humor

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3
Q

what is the fovea?

A

the part of the eye with the highest seeing acute

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4
Q

what is the macula?

A

the space between the superior and inferior retinal arcade (vasculature)

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5
Q

which muscles does CN 3 innervate?

A
  1. superior rectus
  2. inferior rectus
  3. medial rectus
  4. inferior oblique
  5. pupil sphincter (parasympathetic)
  6. levator palpebrae
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6
Q

which muscles does CN 4 innervate?

A

superior oblique

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7
Q

which muscles does CN 6 innervate?

A

lateral rectus

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8
Q

which nerve controls the afferent pathway involving the pupils?

A

CN 2 controls the pathway from your eyes TO your brain

so CN 2 is what brings the light information to the brain

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9
Q

which nerve controls the efferent pathway involving the pupils?

A

CN 3 controls the pathway from your brain TO the eye

so CN 3 is what controls the eye muscles to react to the light

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10
Q

is CN 3 responsible for pupillary constriction or dilation?

A

constriction

it innervates the pupil sphincter!

pupillary constriction is controlled by the parasympathetic nervous system

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11
Q

what is the pupillary reaction to light?

A

if you shine a light in the left eye and everything is normal then the left pupil will constrict because CN 2 sent the information to the brain and then the brain sent information back to the eye via CN 3 to constrict the pupil

the right pupil will also constrict because of the consensual response!

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12
Q

what is an afferent pupillary defect?

A

if both eyes have an afferent pupillary defect and you shine light on the left eye, it won’t constrict because CN 2 is broken! glaucoma is the most common thing to damage CN 2 –> the right eye won’t constrict either because the afferent pathway is broken so there won’t be consensual constricting!

however, if there is an APD in the left eye but your right eye is okay and you shine light in the right eye, the right pupil will constrict AND and the left pupil will also constrict due to consensual response because even though the left afferents are broken, it’s efferents still work!

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13
Q

what is anisocoria?

A

this means the the pupils are different sizes

if you have an APD only in one eye, you WON’T have anisicoria because your efferent fibers are still working so you will have a consensual response that will still cause the broken eye to constrict

however, a condition that can cause one pupil to be smaller than the other is Horner syndrome which knocks out the sympathetic system and allows for uncontrolled parasympathetic responses which constrict your pupils!

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14
Q

which nerves control each of the muscles of the eye?

A

CN 3 controls the superior rectus, medial rectus, inferior rectus and inferior oblique

CN 4 controls the superior oblique

CN 6 controls the lateral rectus

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15
Q

which muscles of the eye will be spared in a retrobulbar block?

A

if you inject anesthetic into the muscular cone, the superior oblique will be the only functional eye muscle because CN 4 is outside the annulus of zenn so your eye will deviate down and out

CN 2, 3 and 6 are inside the annulus of zenn and also the nasociliary nerve (V1) and ophthalmic artery

CN 4, the superior opthalmic vein, frontal nerve and lacrimal nerve are all outside the annulus of zenn but inside the superior orbital fissure

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16
Q

which nerve is effected if a patient is unable to open their eyelid?

A

CN 3

CN 3 controls the levator palpebrae which opens your eye!

the other muscle responsible for opening the eye is the tarsal muscle which is sympathetically controlled so it’s not related to a CN and only does a few mm of eyelid opening –> so people with Horner’s syndrome who have knocked out their sympathetic nervous system will just have a mild ptosis since that knocks out the tarsal muscle but the levator palpebrae still works which does the majority of eye opening

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17
Q

how does CN 4 exit the brain?

A

it exits DORSALLY from the brainstem and travels around to the front to the eyeball so it has the longest intracranial course and is really susceptible to trauma!

CN 4 decussates as it exits the brain stem

note: it is the only cranial nerve to exit dorsally

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18
Q

what does a left-sided trochlear nerve palsy look like?

A

CN 4 = trochlear nerve

if CN 4 is knocked out then the superior oblique is knocked out and the left inferior oblique would be unopposed

this means the eye will be pointed up and out

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19
Q

which disease famously affects the ophthalmic division of the trigeminal nerve?

A

herepes zoster can cause herepes zoster ophthalmicus!

it’s when herpes reemerges as shingles and effects the V1 division of the trigeminal nerve!

this could effect the eyeball because V1 has to do with corneal sensation so shingles could damage the cornea!

the patient will present with what looks like stains on the cornea which are actually inflammation’they’re caratic precipitates which are collections of inflammatory cells that have deposited on the cornea and signify intraoccqular inflammation that’s being caused by the herpes zoster infection!

also the pupil won’t be round which is also caused by the inflammation which has caused the iris to scar down to the lens!! if there’s enough scarring you can block the pathway of aqueous humor out of the eye through the angles and you can get glaucoma too

20
Q

what is CN 6 palsy?

A

CN 6 = abducens nerve which controls the lateral rectus

So if CN 6 is knocked out, the lateral rectus isn’t working so the eyes wouldn’t be about to look outwards

For example, if the left CN 6 isn’t working, that means the left eye lateral rectus is effected and that eye could look to the right but when it tries to look to the left, it would just get stuck in the middle —> however, the right eye would be able to look to the left because it’s CN 6 is fine

21
Q

What is the most common cause of isolated CN 6 palsy?

A

Microvascular ischemia

So like someone with diabetes, hypertension, high cholesterol, or smoking could all effect CN 6 because all these diseases eventually cause strokes and heart attacks because they’re damaging the blood vessels and compromising blood flow to your organs!

22
Q

What are the motor nerves of CN 7?

A
Temporal
Zygomatic
Buccal
Mandibular
Cervical 

“To Zanzibar By Motor Car”

23
Q

How would a facial nerve palsy effect the eye?

A

CN 7 controls the orbicularis oris so you wouldn’t be able to close your eye! You should be worried about chronic dryness which could scar your cornea and cause vision loss

Also, what is often seen is Bell’s phenomenon. So in the eye that can’t close, you will notice that the eye is pointed up. When you normally close your eyes the eyes move up and it’s a protective phenomenon so a person with facial palsy may still have an intact Bell’s reflex even though they can’t close their right eye

24
Q

What is the diagnosis for someone who can’t see the cars around them when they are driving?

A

So this person’s vision quality is totally fine but they can’t see peripherally = bitemporal hemianopsia

The reason the peripheral vision is effected is because usually a pituitary tumor is impinging on the nasal retinal fibers —> the left temporal visual field correlates to the left nasal retina which is being impinged on by the pituitary tumor which is why you can’t see peripherally but your central vision is fine! The temporal fibers stay on the same side and don’t cross over the optic chiasm so they aren’t affected

On a visual field exam, the person would have the peripheral halfs of their vision blacked out = “respecting the vertical midline” which is a classic presentation for this condition

25
Q

What is the most common cause of bitemporal hemianopsia?

A

Pituitary adenoma

If there’s a pituitary tumor, it would impinge on the optic chiasm which would effect BOTH eyes which is why it’s a bitemporal hemianopsia!

26
Q

Will someone with bitemporal hemianopsia have an afferent pupillary defect?

A

No

This is because only the optic tract is being effected, not the optic nerve

27
Q

A 52 year old female comes in with a history of hypertension and has a right sided headache followed by not being able to open the right eye. When you lift up her eye she says she sees double, right pupil is dilated and her eye is pointed down and out. What is the diagnosis?

A

Pupil-involving cranial Nerve 3 Palsy!

Eyelid = ptosis; so the levator palpebrae is not working (CN 3)

Eye = the superior oblique is unopposed because the eye is deviated down and out

Pupils = dilated

THIS IS AN EMERGENCY!!! The symptoms just started, her pupils are involved and CN 3 is being impinged on. This tells you that there is a growing aneurism impinging on the nerve and if it keeps expanding it will pop and you’ll get a subarachnoid bleed!!!! Blood in the brain can give you seizures or herniation of the brain due to increased pressure so it’s just not good

This patient need emergent imaging or neurosurgical intervention to find the aneurism and treat it

28
Q

What often causes a pupil-involving CN 3 palsy?

A

It’s classically due to posterior communicating artery aneurism which is next to CN 3 and compresses on it and damages the nerve

These aneurisms happen because hypertension causes shear stress on the vessels which degrades the integriity of the intracranial vasculature! So this makes you predisposed to aneurisms especially at the branch points because they are weaker due to increased turbulence which increases stress on the vessels!

29
Q

Why are the pupils involved in pupil-involving CN 3 palsy?

A

The pupillary fibers are on the outside of CN 3 so they are easily compressed, like say by a posterior communicating artery aneurism

Specifically, the parasympathetic outputs are on the outside of the nerve while the output to the ocular muscles are more centrally located. So when CN 3 starts to be compressed by an aneurism, the parasympathetic communication will be knocked out and this is normally responsible for pupil constriction —> so without it, the pupil involved will be dilated!

30
Q

A 62 year old female with a history of hypertension, DM2, HLD, CABD x2 and CVA x1 presents with a little bit of a headache and complete ptosis of the right eye. when you lift up the eyelid, she sees double and the eye is deviated down and out but the pupils are the same size. What is the diagnosis?

A

Pupil-sparing cranial nerve 3 palsy

Eyelid = ptosis

Eye = down and out

Pupils = normal

Since it’s pupil-sparing, it means the peripheral parasympathetic fibers of CN 3 are intact while the centrally located motor fibers to the ocular muscles and arteries are the ones being effected so the SR, MR, IR, IO and levator palpebrae will be effected

This is NOT an emergency because it’s just being caused by microvascular ischemia effecting CN 3 so just observe and optimize risk factors like controlling DM 2/HTN —> this will usually resolve itself in a few months

31
Q

Why does a pupil-sparing CN 3 palsy not involve the pupils?

A

Because the pathology is more of an internal problem involving the nerve, not a peripheral problem which involves the parasympathetic fibers that constrict the pupil; it is instead involving the blood vessels inside the nerve

So in this case, the parasympathetic fibers of CN 3 are intact and the pupils are a normal size, the problem is instead with the motor fibers in the middle of the nerve that go to the ocular muscles

32
Q

A 57 year old male presents with pretty blurry vision in both eyes. He has a history of DM 2, A1C of 9.5 with a historical max of 12, and visual acuity is 20/50 in the right eye and 20/100 in the left eye. When you do a dialated exam everything looks pretty okay expect there are little red and white spots in the right retina. What is the diagnosis?

A

The red spots are microaneurisms and the white spots are exudates = lipid reminants!

This is a diabetic macular edema!!

33
Q

How does diabetes effect the eye?

A

In diabetic retinopathy, you have tiny blood vessels that aren’t getting enough oxygen because the vasculature isn’t healthy and as a result your retinal tissue becomes hypoxic

To try and get more oxygen it increases VEGF to try and make more vasculature to get more oxygen

But the problem is that the VEGF in isolation doesn’t produce good blood vessels….so you’ll get vitreous hemorrhage in the retina because these bad blood vessels just break and leak blood into the eye

Another thing VEGF can do is increase vascular permeability which is what gives you the macular edema and blurry vision…..so you have a lot of bad, leaky blood vessels

This abnormal blood vessel formation isn’t just in the retina, it can happen in the cornea too which could give you glaucoma because your angle is blocked off by the blood vessels too

34
Q

What would be the possible fixed vs. transient differentials for sudden, painless, unilateral vision loss?

A

FIXED (don’t go away)

  1. Stroke
  2. Vitreous hemorrhage
  3. Retinal detachment
  4. Central retinal artery occlusion
  5. Central retinal vein occlusion
  6. Cerebrovascular accident

TRANSIENT (goes away)

  1. Migraine
  2. Transient ischemic attack
  3. Transient visual obscurantion
  4. Amaurosis fugax
35
Q

How long do the various transient causes of sudden, painless unilateral vision loss last?

A
  1. Migraine = few hours
  2. Transient ischemic attack (TIA) = less than 24 hours
  3. Transient visual obscurantion = few seconds; it’s idiopathic cranial hypertension associated with TIA
  4. Amaurosis fugax = few minutes
36
Q

What does a dilated exam for a central retinal vein occlusion look like? What causes this?

A

“Blood and thunder”

This is a flame hemorrhage following along the path of the retinal nerve fibers so essentially they’re bleeds on top of the retina

This is due to backed up veins so the blood spills back into the retina —> the central retinal artery and vein share a sheath as they come in through the optic nerve and it’s a tight pathway so if someone has atherosclerotic disease it will compress the artery which will compress the vein and then blood can’t get out of the eye = venous stasis = thrombosis = vein occlusion

Work up may not be necessary if you’re already aware of the risk factors that could be causing this but if there’s no history, then do a hypercoagulable work up

37
Q

What is the most systemic risk factor for developing central retinal vein occlusion?

A

Hypertension!

What if someone comes in with CRVO but they’re 25 and don’t have HTN…they probably have SLE which puts them in a hypercoaguable state

38
Q

65 year old male present with sudden, painless vision loss in their right eye. They have a history of poorly controlled HTN, HPL CABG x2 and CVA x1. Visual acuity in the left eye is 20/20. Dilated exam shows cherry red spot. What is the diagnosis?

A

Central retinal artery occlusion = the blood flow to the CRA is disrupted/occluded and this is an embolia phenomenon from carotid atherosclerotic disease

This dude is 65 and has a lot of vascular risk factors along with unilateral, painless vision loss so basically what’s happening is there isn’t enough blood flow to the retina which is what makes the dilated exam look boggy and edematous

CRAO is a sign of stroke because this means that the person is throwing clots in their arteries and next time instead of it landing in the eye, it could land in the brain and kill them —> so you need to do an urgent stroke work up like EKG, lipid panel, carotid ultrasound and try to do risk factor modifications

39
Q

What is a papilladema vs. optic nerve edema?

A

Papilledema = swelling of the optic nerve secondary to elevated intercranial pressure so it will be bilateral

Optic nerve edema = any kind of optic nerve swelling; can be bilateral or unilateral

40
Q

What does the dilated exam for an optic nerve edema look like?

A

The nerve borders will look blurry where are normal nerves should be pink and sharp

41
Q

84 year old female with no PMH present with lost vision in her left eye and her head hurts. She has had severe headaches for the past few weeks and suddenly lost vision in her left eye two days ago which never returned. VA is 20/20 in the right eye. Dilated eye exam shows an edematous and white nerve. What is the diagnosis?

A

Giant cell arteritis!

The white, chalky appearance of the nerve is classic for GCA!

This is a disease of medium and large sized arteries so it’s a vasculitis = inflammatory disease, NOT a blockage/thrombosis —> so essentially there’s inflammation to the point that the blood vessels become so narrow that blood is barely passing through

The classic place to see this is in the temporal artery which will be bulging to do the backed up pressure and blood

42
Q

What are the 6 classical signs of giant cell arteritis?

A
  1. Fevers
  2. Anorexia
  3. Vision loss
  4. Scalp tenderness
  5. Polymyalsia rheumatica
  6. Over 55 years old

The inflammation will cause fever and chills from the cytokines being released surrounded the inflammation —> there will also be an increased ESR and CRP which are nonspecific signs of inflammation

They will be anorexic because of jaw claudication = pain in their TMJ due to ischemia so then they just don’t eat

Scalp tenderness is because of necrosis of the scalp due to occluded vasculature

Polymyalsia rheumatica is VERY closely related to GCA and in this condition patients can’t raise their hands over their hands

43
Q

How do you treat giant cell arteritis?

A

Steroids

With one inflammed artery you an easily have multiple become occluded as the inflammation spreads so start them on steroids to reduce inflammation and get a temporal artery biopsy to see what’s going on

44
Q

What are the steps of describing an external eye exam?

A
  1. Lids and lashes
  2. Conjunctiva and sclera
  3. Cornea
  4. Anterior chamber
  5. Iris
  6. Lens
45
Q

What are the steps of describing a retinal exam?

A
  1. Media
  2. Optic nerve
  3. Retina
  4. Vessels